Distribution of tenascin in healing incision, excision and laser wounds

Abstract

The distribution of the extracellular matrix glycoprotein, tenascin, was studied in normal mucosa and during healing of scalpel incised or excised and CO2 laser-wounded rat tongue dorsal mucosa in 51 male Sprague-Dawley rats over a period of 21 days. A polyclonal antibody specific for tenascin was applied in indirect immunofluorescence microscopy. In normal mucosa tenascin was sparsely distributed in a discontinuous manner at the tips of the connective tissue papillae in association with the basement membrane (BM) and in the walls of the capillaries. In all the healing wounds there was a marked increase in the distribution of tenascin, particularly close to the BMs at the wound edges beneath the proliferating and migrating epithelium, and later on during healing in the regenerating connective tissue (CT) area. This expression subsided later on during healing. Laser surgery did not alter the ability of fibroblasts to synthesize tenascin. The transient expression of tenascin in the BMs and CT of the healing wounds suggests that this protein could play an important role in providing ideal conditions for cell movement, and in the deposition and organization of other extracellular matrix (ECM) glycoproteins during tissue repair.

Tenascin-C in the cochlea of the developing mouse

“…2B,D), suggesting that these cells may be a source of the protein. In other regions of the nervous system, an increase in tenascin-C is associated with wound healing (Mackie et al, 1988a;Chuong and Chen, 1991;Luomanen and Virtanen, 1993) and with nerve damage or paralysis (Sanes et al, 1986;Daniloff et al, 1989;Gatchalian et al, 1989;Martini et al, 1990;Laywell et al, 1992). We immunolabeled tenascin-C in the cochlea of the Bronx waltzer mouse (Deol and Gluecksohn-Waelsch, 1979;Whitlon and Sobkowicz, 1991;Whitlon et al, 1996), a degenerative mutant in which most inner hair cells die between E17 and P2 along a base-to-apical progression.…”

“…Effects of tenascin-C have been reported on cell growth (Chiquet-Ehrismann et al, 1986), epithelialmesenchymal interactions (Chiquet-Ehrismann et al, 1986Aufderheide et al, 1987;Aufderheide and Ekblom, 1988;Inaguma et al, 1988;Ekblom and Aufderheide, 1989;Vainio et al, 1989), neural development (Crossin et al, 1986;Tan et al, 1987;Mackie et al, 1988b;Halfter et al, 1989), and neuron-glia interactions (Grumet et al, 1985). In most regions, tenascin-C disappears during development, but the molecule can reappear during wound healing (Mackie et al, 1988a;Chuong and Chen, 1991;Luomanen and Virtanen, 1993), after nerve damage or paralysis (Sanes et al, 1986;Daniloff et al, 1989;Gatchalian et al, 1989;Martini et al, 1990;Laywell et al, 1992), or in tumors (Chiquet-Ehrismann et al, 1986;Erickson and Taylor, 1987;Mackie et al, 1987a;Inaguma et al, 1988;Erickson and Bourdon, 1989;Kawakatsu et al, 1992).…”

Tenascin expression in inflammatory, dysplastic and neoplastic lesions of the human stomach

“…Tn has been reported to emerge during wound healing process and disappear when the healing process is complete [3,14,15]. We noted that in gastric and in pyloric/duodenal ulcers, Tn appeared during the process of mucosal regeneration.…”

“…Tn expression is mostly limited to some epithelial-stromal interfaces. However, Tn re-emerges strongly during wound healing [3,14,15], proliferative states [21,28] and in oncogenesis [2], suggesting that it has a role in tissue remodelling.…”

The specific expression of tenascin in the synovial membrane of the temporomandibular joint with internal derangement: An immunohistochemical study

“…TN has also been confirmed to be present during wound healing and tissue repair (Luomanen and Virtanen 1993;Mackie et al 1988).…”